The effects of hourly differences in air pollution on the risk of myocardial infarction: case crossover analysis of the MINAP database

Objectives To investigate associations between air pollution levels and myocardial infarction (MI) on short timescales, with data at an hourly temporal resolution. Design Time stratified case crossover study linking clinical data from the Myocardial Ischaemia National Audit Project (MINAP) with PM10, ozone, CO, NO2, and SO2 data from the UK National Air Quality Archive. Pollution effects were investigated with delays (lags) of 1-6, 7-12, 13-18, 19-24, and 25-72 hours in both single and multi-pollutant models, adjusted for ambient temperature, relative humidity, circulating levels of influenza and respiratory syncytial virus, day of week, holidays, and residual seasonality within calendar month strata. Setting Population based study in 15 conurbations in England and Wales. Subjects 79 288 diagnoses of myocardial infarction recorded over the period 2003-6. Main outcome measures Excess risk of myocardial infarction per 10 mu g/m(3) increase in pollutant level. Results In single pollutant models, PM10 and NO2 levels were associated with a very short term increase in risk of myocardial infarction 1-6 hours later (excess risks 1.2% (95% confidence interval 0.3 to 2.1) and 1.1% (0.3 to 1.8) respectively per 10 mu g/m(3) increase); the effects persisted in multi-pollutant models, though with only weak evidence of an independent PM10 effect (P=0.05). The immediate risk increases were followed by reductions in risk at longer lags: we found no evidence of any net excess risk associated with the five pollutants studied over a 72 hour period after exposure. Conclusions Higher levels of PM10 and NO2, which are typically markers of traffic related pollution, seem to be associated with transiently increased risk of myocardial infarction 1-6 hours after exposure, but later reductions in risk suggest that air pollution may be associated with bringing events forward in time ("short-term displacement") rather than increasing overall risk. The well established effect of air pollution on cardiorespiratory mortality may not be mediated through increasing the acute risk of myocardial infarction, but through another mechanism.